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Modulating Lysine Crotonylation in Cardiomyocytes Improves Myocardial Outcomes

Wenqian Cai1, Dacai Xu1,2, Chui Zeng1

  • 1Heart Center and Institute of Pediatrics (W.C., D.X., C.Z., R.L., Y.L., Y.Z., W.D., Q.W., D.W., J.G., J.W., J.D.), Guangzhou Women and Children's Medical Center, Guangzhou Medical University, China.

Circulation Research
|August 3, 2022
PubMed

Insights

Lysine crotonylation (Kcr) is a key response to cardiac ischemia-reperfusion injury, impacting cardiomyocyte function. Modulating Kcr offers a potential therapeutic target for ischemic heart disease.

Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Ischemic heart disease presents significant global health challenges with limited functional recovery.
  • Lysine crotonylation (Kcr), a post-translational modification, is linked to active gene promoters.
  • The role of Kcr in myocardial injury remains largely unexplored.

Purpose of the Study:

  • To elucidate the pathophysiological significance of Kcr in cardiac injury.
  • To investigate the underlying mechanisms of Kcr in myocardial damage.

Main Methods:

  • Dynamic changes in Kcr sites and protein levels were assessed in left ventricular tissues post-ischemia-reperfusion.
  • Liquid chromatography-coupled tandem mass spectrometry (LC-MS/MS) was employed.
  • Gain- and loss-of-function mutations targeting specific Kcr sites were utilized in vitro and in vivo.

Main Results:

  • Cardiac ischemia-reperfusion injury induced preferential Kcr of proteins involved in cardiomyocyte contractility, including mitochondrial and cytoskeletal proteins.
  • Kcr changes were associated with disrupted cardiomyocyte mitochondrial and sarcomere architecture, autophagy, and apoptosis.
  • Modulating Kcr, specifically of IDH3a and TPM1, or enhancing general Kcr protected cardiomyocytes and preserved myocardial function by inhibiting apoptosis and fibrosis.

Conclusions:

  • Kcr modulation is a critical response of cardiomyocytes to ischemia-reperfusion injury.
  • Targeting Kcr represents a novel therapeutic strategy for ischemic heart disease.
Abstract

Keywords:
autophagycytoskeletonischemialysinemitochondriamyocytes, cardiac

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